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Mid-wavelength infrared HgCdTe avalanche photodiodes (APDs) are becoming increasingly significant in research and practical applications for the high linear gain, low excess noise and high quantum efficiency. However, the performance of HgCdTe APDs is largely limited by the voltage dependence of dark current. It has been well known that the tunneling current is the main component of the dark current of the p-i-n diode. However, the current contribution of different physical mechanism still needs to be indicated in different reverse voltages. In this paper, we mainly study the mechanism of the relationship between dark current and reverse voltage of mid-wavelength infrared Hg 1 - x Cd x Te (x = 0.3) mesa p-i-n avalanche diode. Several physical models are used for the dark current numerical simulation. The results show that for detection of Hg 1 - x Cd x Te mesa p-i-n detector under low temperature, dark current is mainly caused by tunneling current. With the reverse voltage increasing, the main component of dark current turns from trap-assisted tunneling current to direct band-to-band tunneling. The transition voltage is positively related to the energy level difference between trap energy level and conduction band. The results may provide a guideline to improve the performance of the mid-wavelength infrared APD detector by ranking the importance of different structural parameters. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) have been reported to be involved in many important biological processes including proliferation, apoptosis, differentiation, and survival. Recently, nuclear paraspeckle assembly transcript 1 (NEAT1), a novel lncRNA, serves as a crucial regulator in tumors. However, the biological role of NEAT1 in liver fibrosis is largely unknown. In this study, the role of NEAT1 was explored in primary mouse hepatic stellate cells (HSCs) and carbon tetrachloride (CCl)-induced mouse liver fibrosis models. We found that NEAT1 expression was significantly increased in CCl-induced mice and activated HSCs. Loss of NEAT1 suppressed liver fibrosis in vivo and in vitro. Conversely, NEAT1 overexpression accelerated HSC activation, including increased cell proliferation and collagen expression. Further studies indicated that the microRNA-122 (miR-122)-Kruppel-like factor 6 (KLF6) axis was involved in the effects of NEAT1 on HSC activation. The effects of NEAT1 on HSC activation were almost blocked down by miR-122 mimics or KLF6 knockdown. Interestingly, both NEAT1 and KLF6 are targets of miR-122. In addition, miR-122 led to a significant reduction in NEAT1 level while NEAT1 overexpression resulted in the suppression of miR-122 expression. Pull-down assay confirmed a direct interaction between miR-122 and NEAT1. NEAT1 contributes to HSC activation via the miR-122-KLF6 axis. In human fibrotic liver samples, increased NEAT1 levels positively correlated with liver fibrosis markers. In conclusion, we disclose a novel NEAT1-miR-122-KLF6 signaling cascade and its implication in liver fibrosis. Key messages: [ABSTRACT FROM AUTHOR]

Improving the functionality of soft continuum manipulators to expand their application space has always been an important development direction for soft robotics. It remains very challenging to calculate the deformations of soft materials and predict the basic structure of soft fingers under complex objective functions and constraints. This work develops a cable-driven soft robotic gripper with multi-input and multi-output using topology optimization considering geometric nonlinearity, which not only performs adaptive grasping but also enables finer manipulations such as rotating or panning the target. A scheme that can describe adaptive grasping behavior is proposed, which converts the contact between the clamping surface and the object into a boundary condition to circumvent complex contact nonlinearities. An additive hyperelasticity technique is used to overcome numerical instabilities, and the finite element analysis is performed in ANSYS. Numerical simulations and experimental results are performed to demonstrate the effectiveness of the optimization algorithm and to illustrate the application potential of the proposed gripper. [ABSTRACT FROM AUTHOR]

Background: Previously, we reported that microRNA-181b (miR-181b) activates hepatic stellate cells partly through the phosphatase and tensin homolog deleted on chromosome 10 (PTEN)/Akt pathway. Aims: The main objective of this study was to ascertain whether serum miR-181b expression is correlated with that of liver hepatitis B virus (HBV) DNA and disease progression in chronic hepatitis B (CHB) patients. Methods: Serum miR-181b and liver HBV DNA levels were quantified in 64 CHB patients with real-time PCR. Liver fibrosis and necroinflammation were graded according to the Ishak scoring system. Results: Serum miR-181b levels were evaluated in the CHB group, compared with healthy controls. Expression in patients with HBsAg (+) was higher than that in patients with HBsAg (−). Notably, serum miR-181b and liver HBV DNA levels were significantly correlated ( P < 0.05). Serum miR-181 levels were higher in patients with serum HBV DNA > 10 IU/ml ( P = 0.017), histologic activity index (HAI) >8 ( P = 0.001) and fibrosis score >4 ( P < 0.0001). Liver HBV DNA levels were higher in patients with abnormal alanine aminotransferase (ALT) values ( P = 0.004), serum HBV DNA levels > 10 IU/ml ( P = 0.034) and fibrosis score >4 ( P = 0.006). Using multivariate logistic regression analysis, serum miR-181b was identified as an independent predictor of disease progression (OR 4.172, 95 % CI 1.838-9.473, P = 0.009 for HAI >8; OR 5.387, 95 % CI 2.067-14.036, P = 0.001 for fibrosis score >4). Conclusions: Serum miR-181b is correlated with liver and serum HBV DNA levels as well as disease progression in CHB. [ABSTRACT FROM AUTHOR]

To assist emergency management planning and prevention in case of hazardous chemical release into the atmosphere, especially in densely built-up regions with large populations, a multi-scale urban atmospheric dispersion model was established. Three numerical dispersion experiments, at horizontal resolutions of 10 m, 50 m and 3000 m, were performed to estimate the adverse effects of toxic chemical release in densely built-up areas. The multi-scale atmospheric dispersion model is composed of the Weather Forecasting and Research (WRF) model, the Open Source Field Operation and Manipulation software package, and a Lagrangian dispersion model. Quantification of the adverse health effects of these chemical release events are given by referring to the U.S. Environmental Protection Agency's Acute Exposure Guideline Levels. The wind fields of the urban-scale case, with 3 km horizontal resolution, were simulated by the Beijing Rapid Update Cycle system, which were utilized by the WRF model. The sub-domain-scale cases took advantage of the computational fluid dynamics method to explicitly consider the effects of buildings. It was found that the multi-scale atmospheric dispersion model is capable of simulating the flow pattern and concentration distribution on different scales, ranging from several meters to kilometers, and can therefore be used to improve the planning of prevention and response programs. [ABSTRACT FROM AUTHOR]